Adjei A A, Shrestha A K, Castro M, Enriquez F J
Department of Veterinary Science and Microbiology, University of Arizona, Tucson 85721, USA.
Am J Med Sci. 2000 Nov;320(5):304-9. doi: 10.1097/00000441-200011000-00002.
Intestinal infections with the protozoan parasite Cryptosporidium parvum are prevalent in both immunocompetent and immunocompromised hosts. Although C parvum is an important cause of outbreaks and opportunistic infections worldwide, little is known about protective mucosal immune responses. This is in part because animal models of infection are limited to those with genetic or induced immunodeficiencies.
In this report, we isolated immune (primed) or nonimmune (unprimed) intraepithelial lymphocytes (IEL) from BALB/cJ mouse intestines, adoptively transferred them into C parvum-infected severe combined immunodeficient (SCID) mice, and evaluated infection and cell phenotype responses.
Control SCID mice that received no IEL shed large numbers of oocysts throughout the experimental period (day 18 to day 72). Transfer of primed IEL significantly reduced fecal oocyst shedding in recipient SCID mice compared with SCID mice that received unprimed IEL or no IEL. SCID mice transferred with unprimed IEL shed variable numbers of fecal oocysts that increased and decreased in bursts until day 57 after infection. SCID mice transferred with primed IEL exhibited significantly higher proportions of T-cell receptor (TCR) alphabeta+, CD8+, and CD8alphabeta+ EL compared with inoculated SCID mice that received unprimed or no IEL.
We conclude that primed IEL from immunocompetent mice may influence protective mucosal response against cryptosporidiosis when transferred into SCID mice. In addition, the increased percentage of TCR alphabeta+, CD8+, CD8alphabeta+ IEL in recipient SCID mice may reflect mucosal cell populations involved in these responses during chronic C parvum infection.
原生动物寄生虫微小隐孢子虫引起的肠道感染在免疫功能正常和免疫功能低下的宿主中都很普遍。尽管微小隐孢子虫是全球范围内暴发和机会性感染的重要原因,但对保护性黏膜免疫反应却知之甚少。部分原因是感染的动物模型仅限于那些具有遗传或诱导免疫缺陷的模型。
在本报告中,我们从BALB/cJ小鼠肠道中分离出免疫(致敏)或非免疫(未致敏)上皮内淋巴细胞(IEL),将它们过继转移到感染微小隐孢子虫的严重联合免疫缺陷(SCID)小鼠体内,并评估感染情况和细胞表型反应。
未接受IEL的对照SCID小鼠在整个实验期间(第18天至第72天)排出大量卵囊。与接受未致敏IEL或未接受IEL的SCID小鼠相比,致敏IEL的转移显著减少了受体SCID小鼠粪便中卵囊的排出。接受未致敏IEL转移的SCID小鼠排出数量不等的粪便卵囊,在感染后直到第57天,这些卵囊数量呈爆发性增减。与接种未致敏IEL或未接受IEL的SCID小鼠相比,接受致敏IEL转移的SCID小鼠表现出更高比例的T细胞受体(TCR)αβ +、CD8 +和CD8αβ + EL。
我们得出结论,当将免疫功能正常小鼠的致敏IEL转移到SCID小鼠体内时,可能会影响针对隐孢子虫病的保护性黏膜反应。此外,受体SCID小鼠中TCRαβ +、CD8 +、CD8αβ + IEL百分比的增加可能反映了慢性微小隐孢子虫感染期间参与这些反应的黏膜细胞群体。